In fact, recent functional studies revealed that in significant number of patients without a detectable cytogenetic aberration, AML emerges from functional cooperation of multiple alterations (e.g., DNMT3A, TET2, IDH, spliceosome mutations) that are often identified as molecular markers of potential pre-leukemic states such as clonal haematopoiesis of indeterminate potential (CHIP) and myelodysplastic syndromes (MDS) [7]. This evidence concerns the gene TET2 and acute myeloid leukemia.